Recombination between genes encoding major outer surface proteins A and B of Borrelia burgdorferi
Corresponding Author
Patricia A. Rosa
laboratory of Microbial Structure and Function
*Tel. (406) 363 3211; Fax (406) 363 6406.Search for more papers by this authorTom Schwan
Laboratory of Vectors and Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases. National Institutes of Health, Hamilton, Montana 59840, USA.
Search for more papers by this authorCorresponding Author
Patricia A. Rosa
laboratory of Microbial Structure and Function
*Tel. (406) 363 3211; Fax (406) 363 6406.Search for more papers by this authorTom Schwan
Laboratory of Vectors and Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases. National Institutes of Health, Hamilton, Montana 59840, USA.
Search for more papers by this authorSummary
Borrelia burgdorferi causes Lyme disease, a multisystem illness that can persist in humans for many years. We describe recombination between homologous genes encoding the major outer surface proteins (Osps) A and B of B. burgdorferi which both deletes osp gene sequences and creates chimaeric gene fusions. Recombinant osp genes occur in multiple strains and encode unique proteins that lack some characteristic Osp epitopes. Antigenic variation in Osp through recombination may be relevant to the persistence of B. burgdorferi in an infected host, and has important implications for the utility of OspA and OspB as diagnostic or vaccine candidates for Lyme disease. We also describe Osp variation arising from nonsense mutations and sequence divergence, which may also represent significant sources of Osp polymorphism.
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